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87 Cards in this Set
- Front
- Back
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Cardiac Glycosides - Examples
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digoxin/Lanoxin
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Cardiac Glycosides - Indications
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Treatment of arrhythmias, such as atrial fibrillation, atrial flutter, and atrial tachycardia. Treatment of heart failure.
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Cardiac Glycosides - Mechanism of Action
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Cause decreased conduction of electrical activity in cardiac muscle tissue (negative dromotrope), decreased cardiac output), decreased heart rate (negative chronotrope, decreased cardiac output), and increased contractility of cardiac muscle tissue (positive inotrope, increased cardiac output) by decreasing sodium and potassium transport across cell membranes.
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Cardiac Glycosides - Onset of Action/Half-Life
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- digoxin - Half-life is twenty to fifty hours.
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Cardiac Glycosides - Adverse Effects
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Commonly include headache, confusion, disturbed colour vision, bradycardia, ectopic heart beats, and heart blocks, especially AV blocks. Signs of digoxin toxicity include facial pain, weakness, nightmares, confusion, hallucinations, bradycardia, abdominal pain, nausea, and emesis.
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Cardiac Glycosides - Monitoring Requirements
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It is prudent to monitor serum levels of digoxin to maintain them within its narrow therapeutic range, and assess heart rate prior to administering. It is also prudent to monitor serum levels of potassium as hypokalæmia can cause digoxin toxicity.
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Antiplatelet Agents - Examples
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acetylsalicylic acid/Aspirin/Astrix/Cartia/Cardiprin
clopidogrel/Iscover/Plavix dipyridamole/Persantin Combinations - aspirin+clopidogrel/DuoCover |
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Antiplatelet Agents - Indications
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Prevention and treatment of thromboembolic events, such as acute thrombosis, deep vein thrombosis, pulmonary embolism, angina, acute myocardial infarction, stroke, transient ischæmic accident, atrial fibrillation, and post coronary surgery.
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Antiplatelet Agents - Contraindications
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Do not use in patients with active gastrointestinal bleeding or severe liver impairment.
Use with caution in patients who are taking NSAIDs as they can increase the risk of gastrointestinal bleeding, or in patients who are pregnant or breastfeeding. |
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Antiplatelet Agents - Mechanism of Action
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aspirin - Causes decreased platelet stickiness and aggregation ability, and decreased blood viscosity by inhibiting thromboxane.
clopidogrel - Causes decreased platelet aggregation ability by competing with platelets for receptors. |
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Antiplatelet Agents - Adverse Effects
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Commonly include bleeding, diarrhœa, and rashes.
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Antiplatelet Agents - Monitoring Requirements
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Patients taking antiplatelet agents are to report this prior to planned procedures or surgeries so that antiplatelet agents can be slowly stopped to minimise the risk of bleeding during or after the procedure or surgery.
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Thombolytics/Fibrinolytics - Examples
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alteplase/Actilyse
reteplase/Rapilysin streptokinase/Steptase tenecteplase/Metalyse |
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Thombolytics/Fibrinolytics - Indications
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Treatment of thromboembolic events, such as acute thrombosis, deep vein thrombosis, pulmonary embolism, angina, acute myocardial infarction, stroke, transient ischæmic accident, atrial fibrillation, and post coronary surgery.
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Thombolytics/Fibrinolytics - Mechanism of Action
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Cause thrombolysis.
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Thombolytics/Fibrinolytics - Adverse Effects
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Commonly include intracranial, internal, and superficial bleeding, hyposensitivity fever, arrhythmias, and hypotension.
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Thombolytics/Fibrinolytics - Monitoring Requirements
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Thrombolytics require administration as soon as possible after the onset of symptoms and within six to twelve hours of vessel occlusion to be effective. It is prudent to monitor puncture sites for bleeding and avoid intramuscular injections, venepuncture, and rough handling.
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Anticoagulants
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Heparins
Vitamin K Antagonists |
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Heparins - Examples
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heparin
low molecular weight heparin (LMWH)/enoxaparin/Clexane/delteparin/Fragmin |
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Heparins - Indications
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Prevention and treatment of thromboembolic events, such as acute thrombosis, deep vein thrombosis, pulmonary embolism, angina, acute myocardial infarction, stroke, transient ischæmic accident, atrial fibrillation, and post coronary surgery, especially during pregnancy and in cases of extracorporeal circulation.
LMWH - As above but also treatment of unstable angina. |
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Heparins - Mechanism of Action
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Cause augmentation of antithrombin III, and decreased conversion of factor II (prothrombin) into factor IIa (thrombin) and factor I (fibrinogen) into factor Ia (fibrin) by decreasing activity of factor Xa and factor IIa (thrombin) and increasing the effect of antiFactor Xa and antithrombin III.
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Heparins - Onset of Action/Half-Life
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Effective in twenty to thirty minutes, duration three to six hours.
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Heparins - Adverse Effects
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Commonly include hæmorrhage, hæmotoma, local irritation, and mild pain at injection sites, early signs of bleeding, such as bruising, epistaxis, bleeding gums, and heavy menstruation, signs of internal bleeding, such as abdominal pain, hæmoptysis, hæmatemesis, malæna, hæmaturia, dizziness, and thrombocytopænia, increased liver enzyme levels, osteoporosis with long-term high dose use.
Occasionally but rarely include heparin-induced thrombocytopenia (HIT) and heparin-induced thrombocytopenia and thrombosis (HITT). |
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Heparins - Monitoring Requirements
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Heparin is strongly lipophobic and will be broken down by the gut therefore is given intravenously or subcutaneously instead of orally. It is prudent to monitor activated partial thromboplastin time (APTT), the level of time taken for plasma to clot using the intrinsic pathway, six hours after the commencement of treatment and then daily. Normal times range from 26-39 seconds, while times from patients on heparin range from 50-90 seconds. Prolonged APTT can be caused by a deficiency or inhibition of coagulation factors in the intrinsic pathway, specifically I (fibrinogen), II (prothrombin), V, VIII, IX, X, XI and XII, and inhibition can occur due to an anticoagulant, such as heparin. LMWH has a relatively minor effect on APTT. In cases of heparin overdose, protamine sulphate can be used as an antidote to bind to the heparin.
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Vitamin K Antagonists - Examples
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warfarin/Coumadin/Marevan
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Vitamin K Antagonists - Indications
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Prevention and treatment of thromboembolic events, such as acute thrombosis, deep vein thrombosis, pulmonary embolism, angina, acute myocardial infarction, stroke, transient ischæmic accident, atrial fibrillation, and post coronary surgery.
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Vitamin K Antagonists - Contraindications
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Do not use in patients with peptic ulcers, liver disease, or kidney disease.
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Vitamin K Antagonists - Mechanism of Action
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Cause interference with the production of coagulation factors II (prothrombin), VII, IX and X in the liver by competing for enzymes with vitamin K, which is essential to the process.
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Vitamin K Antagonists - Onset of Action/Half-Life
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Effective in thirty-six to seventy-two hours, duration four to five days after discontinuation.
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Vitamin K Antagonists - Adverse Effects
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Commonly include fever, hypersensitivity reaction, hæmorrhage, early signs of bleeding, such as epistaxis and bleeding gums, nausea, emesis, diarrhœa, and alopecia.
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Vitamin K Antagonists - Drug Interactions
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Effect is increased by antibiotics, aspirin, alcohol, cimetidine, dipyridamole and phenytoin.
Effect is decreased by barbituates. |
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Vitamin K Antagonists - Monitoring Requirements
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It is prudent to monitor prothrombin time (PT), the level of time taken for plasma to clot using the extrinsic pathway. The time taken to clot is mathematically processed to produce an international normalised ratio (INR) which can then be interpreted. Normal values range from 1.0-1.3, while values from patients on warfarin range from 2.0-4.0. Prolonged or high INR can be caused by a deficiency or inhibition of coagulation factors in the extrinsic pathway, specifically I (fibrinogen), II (prothrombin), V, VII and X, and inhibition can occur due to an anticoagulant, such as warfarin. In cases of warfarin overdose, vitamin K can be used as an antidote. Patients taking warfarin are to report this prior to planned procedures or surgeries so that warfarin can be slowly stopped to minimise the risk of bleeding during or after the procedure or surgery, and are to have identification, such as a medic bracelet, to alert healthcare professionals that they are taking warfarin.
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Antianginals - Nitrates - Examples
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glyceryl trinitrate/Anginine/Lycinate/Minitran/Nitro-Dur/Transiderm-Nitro/Nitrolingual
isosorbide mononitrate/Duride/Imdur/Monodur/Intrate SR isosorbide dinitrate/Isordil/Sorbidin |
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Antianginals - Nitrates - Indications
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Treatment of angina.
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Antianginals - Nitrates - Mechanism of Action
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Cause decreased oxygen demand in cardiac muscle tissue by causing vasodilation, decreasing blood pressure, increasing heart rate, decreasing preload, and decreasing afterload.
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Antianginals - Nitrates - Adverse Effects
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Commonly include headache, dizziness, blurred vision, restlessness, palpitations, hypotension, reflex tachycardia, facial flushing, dry mouth, abdominal pain, and emesis.
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Antianginals - Nitrates - Monitoring Requirements
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It is prudent to assess blood pressure prior to administering and during action. Patients are to administer sprays or tablets under the tongue as first symptoms occur and advised to sit until symptoms subside. If no improvement occurs, a second and third dose are to be administered five minutes after the previous dose, but if no improvement occurs after three doses then emergency services are to be called. If using a spray, discard after expiry date, if using tablets, discard after ninety days due to loss of potency, and if using a patch, nurses are to write the date and time on the patch itself and avoid contact with the drug as it can be absorbed through the skin.
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Antihypertensives
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Alpha Receptor Antagonists
Angiotensin Converting Enzyme Inhibitors Angiotensin II Receptor Blockers Beta Receptor Antagonists Calcium Channel Blockers Peripheral Vasodilators |
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Alpha Receptor Blockers - Examples
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prazosin/Minipress
terazosin/Hytrin |
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Alpha Receptor Blockers - Indications
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Treatment of hypertension.
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Alpha Receptor Blockers - Contraindications
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Do not use in patients with congestive heart failure caused by aortic or bicuspid valve stenosis, pulmonary embolism, or when a fall in blood pressure is undesirable.
Use with caution in patients with ischæmic heart disease, angina, cerebral arteriosclerosis, coronary arteriosclerosis. |
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Alpha Receptor Blockers - Mechanism of Action
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Cause vasodilation and decreased systemic vascular resistance by competing with catecholamines for alpha receptors in arterioles and venules.
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Alpha Receptor Blockers - Adverse Effects
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Commonly include headache, blurred vision, drowsiness, dizziness, syncope, weakness, fatigue, hypotension, dry mouth, nausea, emesis, rashes, and pruritis, especially after the first dose, after an increase in dosage, or after an interruption to regimen.
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Alpha Receptor Blockers - Drug Interactions
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Effect is increased by antipsychotics.
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Alpha Receptor Blockers - Monitoring Requirements
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It is prudent to assess blood pressure prior to administering. Consider giving the first dose prior to sleep to prevent adverse effects related to the first dose.
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Angiotensin Converting Enzyme Inhibitors - Examples
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captopril/Capoten/Acenorm
enalapril/Vasotec/Renitec fosinopril/Monace/Monopril lisinopril/Zestril/Prinivil/Liprace perindopril/Coversyl quinipril/Accupril ramipril/Tritace |
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Angiotensin Converting Enzyme Inhibitors - Indications
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Treatment of hypertension.
Protective effect against congestive heart failure, acute myocardial infarction, and peripheral vascular disease. |
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Angiotensin Converting Enzyme Inhibitors - Mechanism of Action
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Cause decreased fluid and electrolyte reabsorption in the kidneys, decreased circulating blood volume, vasodilation, and decreased systemic vascular resistance by inhibiting angiotension converting enzyme.
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Angiotensin Converting Enzyme Inhibitors - Adverse Effects
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Commonly include headache, dizziness, palpitations, chest pain, blood dyscrasias, hypotension, tachycardia, dry cough, taste disturbance, gastrointestinal disturbance, progressive kidney impairment, hyperkalæmia, painful joints, and rashes.
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Angiotensin Converting Enzyme Inhibitors - Monitoring Requirements
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It is prudent to assess blood pressure prior to administering, and monitor serum levels of electrolytes.
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Angiotensin II Receptor Antagonists - Examples
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candesartan/Atacand
irbesartan/Karvea/Avapro losartan/Cozaar telmisartan/Micardis valsartan/Diovan |
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Angiotensin II Receptor Antagonists - Indications
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Treatment of hypertension and heart failure.
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Angiotensin II Receptor Antagonists - Mechanism of Action
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Cause vasodilation and decreased systemic vascular resistance by competing with angtiotensin II for angiotensin II receptors.
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Angiotensin II Receptor Antagonists - Adverse Effects
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Commonly include headache, dizziness, insomnia, hypotension, rhinitis, abdominal pain, and gastrointestinal disturbance.
Rarely include hyperkalæmia. |
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Angiotensin II Receptor Antagonists - Monitoring Requirements
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It is prudent to assess blood pressure prior to administering, and monitor serum levels of electrolytes
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Beta Receptor Antagonists - Examples
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Beta1 Selective Antagonists
atenolol/Tenormin/Noten esmolol/Brevibloc metoprolol/Betaloc/Lopessor Non-Selective Antagonists carvedilol/Coreg nadolol/Corgard oxprenalolol/Corbeton propranolol/Inderal pindolol/Visken sotalol/Cardol/Sotacor |
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Beta Receptor Antagonists - Indications
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Treatment of hypertension.
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Beta Receptor Antagonists - Contraindications
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Use with caution in patients with asthma, bronchospasm and chronic obstructive airways disease.
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Beta Receptor Antagonists - Mechanism of Action
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Cause decreased oxygen demand in cardiac muscle tissue, vasodilation, decreased systemic vascular resistance, decreased conduction of electrical activity in cardiac muscle tissue (negative dromotrope, decreased cardiac output), decreased heart rate (negative chronotrope, decreased cardiac output), decreased contractility of cardiac muscle tissue (negative inotrope, decreased cardiac output), and decreased blood glucose levels by competing with catecholamines for beta receptors.
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Beta Receptor Antagonists - Adverse Effects
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Commonly include headache, dizziness, fatigue, sleep disturbance, insomnia, postural hypotension, bradycardia, heart blocks, especially AV blocks, bronchospasm, abdominal pain, gastrointestinal disturbance, hypoglycæmia, sweating, and rashes.
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Beta Receptor Antagonists - Monitoring Requirements
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It is prudent to monitor heart rate and blood pressure, monitor blood glucose levels in diabetics, be aware of postural hypotension and advise patients to sit or lie if dizzy. Slowly decrease dose when stopping treatment to decrease risk of arrhythmias, angina, and acute myocardial infarction.
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Calcium Channel Antagonists - Examples
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amlodipine/Norvasc
felodipine/Plendil nifedipine/Procardia/Adalat diltiazem/Cardizem verapamil/Isoptin/Cordilox |
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Calcium Channel Antagonists - Indications
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Treatment of hypertension.
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Calcium Channel Antagonists - Mechanism of Action
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Cause vasodilation in small arteries, decreased systemic vascular resistance, decreased conduction of electrical activity in cardiac muscle tissue (negative dromotrope, decreased cardiac output), decreased heart rate (negative chronotrope, decreased cardiac output), and decreased contractility of cardiac muscle tissue (negative inotrope, decreased cardiac output) by decreasing calcium channel activity and decreasing
calcium transport across cell membranes. |
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Calcium Channel Antagonists - Adverse Effects
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Commonly include headache, dizziness, hypotension, œdema, dry mouth, taste disturbance, gingival hyperplasia, diarrhœa, and constipation
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Calcium Channel Antagonists - Monitoring Requirements
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It is prudent to monitor heart rate and blood pressure.
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Peripheral Vasodilators - Examples
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diazoxide
hydralazine/Alphapress/Apresoline minoxidil/Loniten sodium nitroprusside |
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Peripheral Vasodilators - Indications
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Emergency treatment of hypertension.
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Peripheral Vasodilators - Mechanism of Action
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Cause vasodilation and decreased systemic vascular resistance.
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Antiarrhythmics
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Class I
Class II - Beta Receptor Antagonists Class II Class IV - Calcium Channel Antagonists |
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Class I Antiarrhythmics - Examples
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disopyramide/Rythmodan
quinidine bisulphate/Kinidin Durules lignocaine/Xylocard phenytoin/Dilantin mexiletine/Mexitil flecainide/Flecatab/Tambocor |
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Class I Antiarrhythmics - Indications
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Treatment of arrhythmias.
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Class I Antiarrhythmics - Mechanism of Action
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Cause slow repolarisation during action potentials by decreasing sodium channel activity and reinflux of sodium.
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Class III Antiarrhythmics - Examples
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amiodarone/Cordarone
sotolol/Sotacor |
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Class III Antiarrhythmics - Indications
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Treatment of arrhythmias.
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Class III Antiarrhythmics - Mechanism of Action
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Cause increased action potential duration
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Antilipids
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HMG-CoA Reductase Inhibitors
Bile Acid-Binding Agents |
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HMG-CoA Reductase Inhibitors - Examples
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atorvastatin/Lipitor
fluvastatin/Lescol/Vastin pravastatin/Pravachol simvastatin/Lipex/Zocor |
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HMG-CoA Reductase Inhibitors - Indications
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Treatment of hyperlipidæmia and atherosclerosis.
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HMG-CoA Reductase Inhibitors - Mechanism of Action
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Cause decreased cholesterol synthesis in the liver, increased low density lipoprotein receptor expression in the liver, increased low density lipoprotein binding in the liver, and increased cholesterol uptake by the liver by inhibiting HMG-CoA reductase
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HMG-CoA Reductase Inhibitors - Adverse Effects
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Commonly include headache, dizziness, insomnia, stomach upset, stomach pain, nausea, flatulence, diarrhœa, constipation, gynæcomastia, myalgia, myopathy, alopecia, and rashes.
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HMG-CoA Reductase Inhibitors - Drug Interactions
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Effect is increased by grapefruit juice. Patients on statins are to avoid large levels of grapefruit juice as they are metabolised by the same enzyme and this competition can cause higher level of statins to accumulate in the body.
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HMG-CoA Reductase Inhibitors - Monitoring Requirements
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It is prudent to monitor lipid and hepatic function levels regularly and withhold drug if any metabolic, electrolyte, or endocrine imbalances are observed.
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Bile Acid-Binding Agents - Examples
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cholestyramine/Questran Lite
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Bile Acid-Binding Agents - Indications
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Treatment of hyperlipidæmia, especially hypercholesterolæmia related to increased low density lipoprotein levels, and atherosclerosis.
Prevention of ischæmic heart disease. |
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Bile Acid-Binding Agents - Mechanism of Action
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Cause decreased bile acid reabsorption by binding to bile acids
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Bile Acid-Binding Agents - Adverse Effects
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Commonly include increased bleeding tendency, decreased absorption of lipophilic vitamins, gastrointestinal disturbance, constipation, and osteoporeosis.
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